The concept is simple enough, but the process isn't. Postdoc Chris Waters has been studying how the auto-inducers work in Vibrio cholerae, a V. harveyi relative and, yes, a human pathogen. The funny thing about V. cholerae is that its signals behave almost exactly opposite to those in most bacteria. This bacterium doesn't wait until it's swimming in a critical mass of fellow bacteria to turn on virulence. It's virulent from the get-go; it attacks immediately. What Waters would really like to do is trace the early-stage signals V. cholerae uses and figure out a way to interfere with them. If he could do that, the strategy could then be used on a lot of different pathogens. "It could be something simple like an amino acid or a sugar," Waters says. "You might not need a complex drug to treat illness."

That V. cholerae is a germ that gets humans sick is one reason Waters is working with it and not with V. harveyi. Another reason is Bassler. She wants her students to have their own research they can take with them when they leave so that they can compete with her for grant money - and win. If their research is too much like hers, she'll beat them every time.

Take Federle, the postdoc whose bacterium of choice is strep, the familiar pathogen that causes strep throat and scarlet fever. He's working on mucking up strep's ability to make AI-2 so the germ can't get the message that it's time to go virulent. "If we come up with inhibitors, we could alter their ability to cause disease," Federle says. "That's the ultimate promise of quorum sensing. We identify how they talk, and then, if we mess with their communication, we change their behavior."